Evidence map›Paper›PMID 12933833›Full record

ArticleInfection and immunity2003

Mice lacking inducible nitric oxide synthase demonstrate impaired killing of Porphyromonas gingivalis.

Robert Gyurko, Gabriel Boustany, Paul L Huang, Alpdogan Kantarci, Thomas E Van Dyke, Caroline A Genco, Frank C Gibson

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 52 citations in OpenAlex.

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  12. Signaling mechanisms involved in altered function of macrophages from diet-induced obese mice affect immune responses.Proceedings of the National Academy of Sciences of the United States of America · 2009
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Robert GyurkoDepartment of Periodontology and Oral Biology, Goldman School of Dental Medicine, Boston University, Massachusetts 02118, USA. gyurko@bu.edu
Gabriel Boustany
Paul L Huang
Alpdogan Kantarci
Thomas E Van Dyke
Caroline A Genco
Frank C Gibson
Boston University · USMassachusetts General Hospital · USUniversity Medical Center · US

Funding

P. gingivalis host interactions in vivoP01DE013191 · NIDCR · BOSTON MEDICAL CENTER · PI AMAR, SALOMON · 2000 to 2004
$4.3M
GINGIPAIN R1 PEPTIDES FOR ORAL IMMUNIZATIONR01DE012517 · NIDCR · BOSTON MEDICAL CENTER · PI GENCO, CAROLINE A · 1999 to 2002
$910k
Nitric Oxide Defense Against Porphyromonas gingivalisK22DE014568 · NIDCR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GYURKO, ROBERT · 2003 to 2006
$564k
ORAL IMMUNIZATION WITH GINGIPAIN DELIVERED BY SALMONELLAF32DE005739 · NIDCR · BOSTON MEDICAL CENTER · PI GIBSON, FRANK C · 2000 to 2001
$90k
NHLBI NIH HHS HLS7818NIDCR NIH HHS 1 K22 DE 14568-01A1NIDCR NIH HHS DE 13191NIDCR NIH HHS F32 DE005739NIDCR NIH HHS F32-DE05739NIDCR NIH HHS K22 DE014568NIDCR NIH HHS P01 DE013191NIDCR NIH HHS P01-DE13191NIDCR NIH HHS R01-DE12517
6 · The paper itself

Abstract

Porphyromonas gingivalis is a primary etiological agent of generalized severe periodontitis, and emerging data suggest the importance of reactive oxygen and nitrogen species in periodontal tissue damage, as well as in microbial killing. Since nitric oxide (NO) released from inducible NO synthase (iNOS) has been shown to possess immunomodulatory, cytotoxic, and antibacterial effects in experimental models, we challenged iNOS-deficient (iNOS(-/-)) mice with P. gingivalis by using a subcutaneous chamber model to study the specific contribution of NO to host defense during P. gingivalis infection. iNOS(-/-) mice inoculated with P. gingivalis developed skin lesions and chamber rejection with higher frequency and to a greater degree than similarly challenged C57BL/6 wild-type (WT) mice. Chamber fluid from iNOS(-/-) mice possessed significantly more P. gingivalis than that of WT mice. The immunoglobulin G responses to P. gingivalis in serum was similar in WT and iNOS(-/-) mice, and the inductions of tumor necrosis factor alpha, interleukin-1 beta and interleukin-6, and prostaglandin E(2) were comparable between the two mouse strains. Although no differences in total leukocyte counts in chamber fluids were observed between iNOS(-/-) and WT mice, the percentage of dead polymorphonuclear leukocytes (PMNs) was significantly greater in iNOS(-/-) mouse chamber fluids than that of WT samples. Interestingly, casein-elicited PMNs from iNOS(-/-) mice released more superoxide than did WT PMNs when stimulated with P. gingivalis. These results indicate that modulation of superoxide levels is a mechanism by which NO influences PMN function and that NO is an important element of the host defense against P. gingivalis.

Indexed as

AnimalsAntibodies, BacterialBacteroidaceae InfectionsColony Count, MicrobialCytokinesCytotoxicity, ImmunologicDiffusion Chambers, CultureDinoprostoneFemaleHumansImmunoglobulin GInflammation MediatorsMiceMice, Inbred C57BLMice, KnockoutNeutrophilsAntibodies, BacterialCytokinesDinoprostoneImmunoglobulin GInflammation MediatorsNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type IINOS2 protein, humanNos2 protein, mouseSuperoxides

Identifiers

PMID12933833
PMCPMC187326
OpenAlexW2171369572

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.